Methamphetamine injection during pregnancy decreases STIM1 in different brain regions of male rat’s offspring

Publish Year: 1398
نوع سند: مقاله کنفرانسی
زبان: English
View: 348

نسخه کامل این Paper ارائه نشده است و در دسترس نمی باشد

  • Certificate
  • من نویسنده این مقاله هستم

استخراج به نرم افزارهای پژوهشی:

لینک ثابت به این Paper:

شناسه ملی سند علمی:

TOXICOLOGY15_111

تاریخ نمایه سازی: 15 بهمن 1398

Abstract:

Introduction: Methamphetamine (Meth) exposure not only has an effect on pregnant women but also affects the fetus directly [1]. Particularly, approximately 50% of the Meth abusing population are women [2]. Although the adverse effects of METH are well-described in adults, there is only limited knowledge regarding the impact of METH in pregnant women [3]. The aim of this study was to investigate calcium release form intracellular calcium stored, following prenatal Meth exposure, in the rat’s offspring through measurement of STIM1 [4]. Methods: Female Wistar rats, weighing an average of 200 were used. All rats were kept in temperature-controlled room (25±10), on a 12 h (light): 12 h (dark) cycle. Female rats were housed with male rats and there was always two females one male per cage. From the day 10 to 20 of gestation female rats were intraperitoneally injected with Meth (2 and 5 mg/kg) at 10 a.m. per day. Pups were sacrificed 8 to 10 weeks after birth then STIM1 levels in the Hippocampus, Amygdala and Prefrontal areas were measured via western blotting test.Results: We observed molecular changes in the Hippocampus, Amygdala and Prefrontal of rats prenatally exposed to Meth. Data have shown that STIM1 level decreased in prenatally Meth treatment in comparison control group. Statistical analysis revealed that there were significant difference in the STIM1 level in Hippocampus (P<0.0001), Amygdala (P<0.0001) and in Prefrontal (P=0.0045) between groups.Conclusion: Our data demonstrated that treatment with Meth decreases STIM1 levels and as STIM1 is a key regulator of Ca2+ channels therefore it interferes with calcium release from intracellular calcium stores.

Authors

Romina Tavassoli

Neuroscience Research Center, Shahid Beheshti University of Medical Science, Tehran, Iran

Zahra Pourmanochehri

Neuroscience Research Center, Shahid Beheshti University of Medical Science, Tehran, Iran

Paria Agha Mohammad Hassani

Neuroscience Research Center, Shahid Beheshti University of Medical Science, Tehran, Iran

Parinaz Etemadi

Neuroscience Research Center, Shahid Beheshti University of Medical Science, Tehran, Iran

Nayereh Zare

Islamic Azad University, Medical Branch, Tehran, Iran

Fariba Khodagholi

Neuroscience Research Center, Shahid Beheshti University of Medical Science, Tehran, Iran